| First Author | Powolny-Budnicka I | Year | 2011 |
| Journal | Immunity | Volume | 34 |
| Issue | 3 | Pages | 364-74 |
| PubMed ID | 21419662 | Mgi Jnum | J:169863 |
| Mgi Id | MGI:4943366 | Doi | 10.1016/j.immuni.2011.02.019 |
| Citation | Powolny-Budnicka I, et al. (2011) RelA and RelB Transcription Factors in Distinct Thymocyte Populations Control Lymphotoxin-Dependent Interleukin-17 Production in gammadelta T Cells. Immunity 34(3):364-74 |
| abstractText | The NF-kappaB transcription factor regulates numerous immune responses but its contribution to interleukin-17 (IL-17) production by T cells is largely unknown. Here, we report that IL-17, but not interferon-gamma (IFN-gamma), production by gammadelta T cells required the NF-kappaB family members RelA and RelB as well as the lymphotoxin-beta-receptor (LTbetaR). In contrast, LTbetaR-NF-kappaB signaling was not involved in the differentiation of conventional alphabeta Th17 cells. Impaired IL-17 production in RelA- or RelB-deficient T cells resulted in a diminished innate immune response to Escherichia coli infection. RelA controlled the expression of LT ligands in accessory thymocytes whereas RelB, acting downstream of LTbetaR, was required for the expression of RORgammat and RORalpha4 transcription factors and the differentiation of thymic precursors into gammadeltaT17 cells. Thus, RelA and RelB within different thymocyte subpopulations cooperate in the regulation of IL-17 production by gammadelta T cells and contribute to the host's ability to fight bacterial infections. |
